TY - JOUR
T1 - Suppression of gene amplification and chromosomal DNA integration by the DNA mismatch repair system
AU - Lin, Ching Tai
AU - Lyu, Yi Lisa
AU - Xiao, Hai
AU - Lin, Wei Hsin
AU - Whang-Peng, Jacqueline
PY - 2001/8/15
Y1 - 2001/8/15
N2 - Mismatch repair (MMR)-deficient cells are shown to produce > 15-fold more methotrexate-resistant colonies than MMR normal cells. The increased resistance to methotrexate is primarily due to gene amplification since all the resistant clones contain double-minute chromosomes and increased copy numbers of the DHFR gene. In addition, integration of linearized or retroviral DNAs into chromosomes is also significantly elevated in MMR-deficient cells. These results suggest that in addition to microsatellite instability and homeologous recombination, MMR is also involved in suppression of other genome instabilities such as gene amplification and chromosomal DNA integration.
AB - Mismatch repair (MMR)-deficient cells are shown to produce > 15-fold more methotrexate-resistant colonies than MMR normal cells. The increased resistance to methotrexate is primarily due to gene amplification since all the resistant clones contain double-minute chromosomes and increased copy numbers of the DHFR gene. In addition, integration of linearized or retroviral DNAs into chromosomes is also significantly elevated in MMR-deficient cells. These results suggest that in addition to microsatellite instability and homeologous recombination, MMR is also involved in suppression of other genome instabilities such as gene amplification and chromosomal DNA integration.
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U2 - 10.1093/nar/29.16.3304
DO - 10.1093/nar/29.16.3304
M3 - Article
C2 - 11504867
AN - SCOPUS:0035880770
SN - 0305-1048
VL - 29
SP - 3304
EP - 3310
JO - Nucleic Acids Research
JF - Nucleic Acids Research
IS - 16
ER -